Heat Shock Pretreatment Influences the Expression of PKC Isoforms during Sepsis

Protein Kinase C (PKC) plays a central role in signal transduction and participates in diverse biological and biochemical functions. PKC dysfunction leads to general immunosuppression that, in turn, increases host susceptibility to infection and sepsis. In our previous study, we demonstrated that th...

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Bibliographic Details
Published in:The Journal of surgical research 2001-12, Vol.101 (2), p.202-209
Main Authors: Chen, Hsiang-Wen, Hsu, Chin, Hsu, Hseng-Kuang, Lu, Tzong-Shi, Wang, Shu-Jung, Yang, Rei-Cheng
Format: Article
Language:English
Subjects:
Animal infectious diseases
Animals
Biological and medical sciences
cecal ligation and puncture
General aspects
heat shock protein
Heat-Shock Proteins - analysis
Hot Temperature
HSP72 Heat-Shock Proteins
Infectious diseases
Isoenzymes - analysis
isoform
lymphocyte
Lymphocytes - enzymology
Male
Medical sciences
protein kinase C
Protein Kinase C - analysis
rat
Rats
Rats, Sprague-Dawley
sepsis
Sepsis - enzymology
Tropical medicine
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Summary:Protein Kinase C (PKC) plays a central role in signal transduction and participates in diverse biological and biochemical functions. PKC dysfunction leads to general immunosuppression that, in turn, increases host susceptibility to infection and sepsis. In our previous study, we demonstrated that the mortality of sepsis is significantly decreased in rats treated with heat shock. It was considered that the modulation of PKC content by previous heat shock might contribute to the resistance to a severe infection. In this study, we attempted to understand the change of various PKC isoforms in the lymphocytes during sepsis and to investigate the role of previous heat shock in influencing PKC expression. Cecal ligation and puncture (CLP) was used as the experimental sepsis model for its biphasic clinical manifestation. Heat shock protein and PKC isoforms were detected by immunochemical study. Ten PKC isoforms (α, β, γ, δ, ε, ζ, θ, ι, λ, and μ) were detected from peripheral lymphocytes. Results showed that all the PKC isoforms have a declination tendency along with the progression of CLP-induced sepsis, and previous heat shock treatment could prevent the declination of PKC content, particularly the isoforms β, γ, and ε, during sepsis. We suggest that heat shock response may participate in maintenance of PKC expression and contribute to decrease the severity of systemic infection.
ISSN:0022-4804
1095-8673
DOI:10.1006/jsre.2001.6273